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Bachem damgo
Relative efficacy values for <t>DAMGO,</t> <t>etorphine,</t> endomorphin-2, and morphine for five MOPr signaling outputs. Values refer to efficacy relative to that of DAMGO, which was set to 1.00 for each output. The values for [ 35 S]GTPγS binding and arrestin-3
Damgo, supplied by Bachem, used in various techniques. Bioz Stars score: 92/100, based on 13 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/damgo/product/Bachem
Average 92 stars, based on 13 article reviews
Price from $9.99 to $1999.99
damgo - by Bioz Stars, 2020-09
92/100 stars

Images

1) Product Images from "Endomorphin-2: A Biased Agonist at the ?-Opioid Receptor"

Article Title: Endomorphin-2: A Biased Agonist at the ?-Opioid Receptor

Journal: Molecular Pharmacology

doi: 10.1124/mol.112.078659

Relative efficacy values for DAMGO, etorphine, endomorphin-2, and morphine for five MOPr signaling outputs. Values refer to efficacy relative to that of DAMGO, which was set to 1.00 for each output. The values for [ 35 S]GTPγS binding and arrestin-3
Figure Legend Snippet: Relative efficacy values for DAMGO, etorphine, endomorphin-2, and morphine for five MOPr signaling outputs. Values refer to efficacy relative to that of DAMGO, which was set to 1.00 for each output. The values for [ 35 S]GTPγS binding and arrestin-3

Techniques Used: Binding Assay

Concentration-response curves for activation of the GIRK current in rat LC neurons by DAMGO, etorphine, and endomorphin-2. In individual LC neurons, concentration-response curves for DAMGO ( n = 3–5) (A), etorphine ( n = 3–8) (B),and endomorphin-2
Figure Legend Snippet: Concentration-response curves for activation of the GIRK current in rat LC neurons by DAMGO, etorphine, and endomorphin-2. In individual LC neurons, concentration-response curves for DAMGO ( n = 3–5) (A), etorphine ( n = 3–8) (B),and endomorphin-2

Techniques Used: Concentration Assay, Activation Assay

2) Product Images from "Distinct roles of exogenous opioid agonists and endogenous opioid peptides in the peripheral control of neuropathy-triggered heat pain"

Article Title: Distinct roles of exogenous opioid agonists and endogenous opioid peptides in the peripheral control of neuropathy-triggered heat pain

Journal: Scientific Reports

doi: 10.1038/srep32799

Effects of exogenous opioid receptor agonists on heat hypersensitivity in wild-type and opioid peptide-lacking mice. DAMGO, DPDPE and U50, 488H were injected at the CCI site on days 2 and 14 following CCI, and effects were assessed 5 min after injection using Hargreaves test, in hind paws ipsilateral to the CCI of wild-type, END-KO, PENK-KO or PDYN-KO mice. Dashed lines represent latencies determined before CCI. # P
Figure Legend Snippet: Effects of exogenous opioid receptor agonists on heat hypersensitivity in wild-type and opioid peptide-lacking mice. DAMGO, DPDPE and U50, 488H were injected at the CCI site on days 2 and 14 following CCI, and effects were assessed 5 min after injection using Hargreaves test, in hind paws ipsilateral to the CCI of wild-type, END-KO, PENK-KO or PDYN-KO mice. Dashed lines represent latencies determined before CCI. # P

Techniques Used: Mouse Assay, Injection

3) Product Images from "Role of G Protein–Coupled Receptor Kinases 2 and 3 in μ"

Article Title: Role of G Protein–Coupled Receptor Kinases 2 and 3 in μ

Journal: Molecular Pharmacology

doi: 10.1124/mol.115.098293

Inhibition of MOPr desensitization by Cmpd101 in rat LC neurons. Traces in (A), (D), (G), and (J) show outward potassium currents recorded from rat LC neurons in response to receptor-saturating concentrations of Met-Enk (30 μ M), DAMGO (10 μ M), endomorphin-2 (10 μ M), and morphine (morph; 30 μ M). The Met-Enk, DAMGO, and endomorphin-2 responses desensitized rapidly over the 10 minutes of agonist application. The desensitization induced by morphine was less than that produced by the other agonists and was measured after 15 minutes of morphine application. Agonist responses returned to baseline after washout (Met-Enk) or when naloxone (nalox; 1 μ M) was applied. The middle column of traces, (B), (E), (H), and (K), show currents induced by each agonist in slices exposed to Cmpd101 (30 μ M) for at least 15 minutes before and during the application of the opioid agonists. Traces in (C), (F), (I), and (L) show pooled data for the percentage desensitization after 10 minutes of Met-Enk, DAMGO, or endomorphin-2 application and 15 minutes of morphine application from experiments such as those illustrated in the two columns of experimental traces. Cmpd101 significantly inhibited the desensitization of all four agonists. Met-Enk: n = 5 for all experiments; DAMGO: n = 4 for all experiments; endomorphin-2: n = 6 for all experiments; morphine: n = 6 for all experiments. * P
Figure Legend Snippet: Inhibition of MOPr desensitization by Cmpd101 in rat LC neurons. Traces in (A), (D), (G), and (J) show outward potassium currents recorded from rat LC neurons in response to receptor-saturating concentrations of Met-Enk (30 μ M), DAMGO (10 μ M), endomorphin-2 (10 μ M), and morphine (morph; 30 μ M). The Met-Enk, DAMGO, and endomorphin-2 responses desensitized rapidly over the 10 minutes of agonist application. The desensitization induced by morphine was less than that produced by the other agonists and was measured after 15 minutes of morphine application. Agonist responses returned to baseline after washout (Met-Enk) or when naloxone (nalox; 1 μ M) was applied. The middle column of traces, (B), (E), (H), and (K), show currents induced by each agonist in slices exposed to Cmpd101 (30 μ M) for at least 15 minutes before and during the application of the opioid agonists. Traces in (C), (F), (I), and (L) show pooled data for the percentage desensitization after 10 minutes of Met-Enk, DAMGO, or endomorphin-2 application and 15 minutes of morphine application from experiments such as those illustrated in the two columns of experimental traces. Cmpd101 significantly inhibited the desensitization of all four agonists. Met-Enk: n = 5 for all experiments; DAMGO: n = 4 for all experiments; endomorphin-2: n = 6 for all experiments; morphine: n = 6 for all experiments. * P

Techniques Used: Inhibition, Produced

Related Articles

other:

Article Title: Functional selectivity and time-dependence of μ-opioid receptor desensitization at nerve terminals in the mouse ventral tegmental area
Article Snippet: Materials The compounds used in these experiments were supplied as shown below: DAMGO and Met-enkephalin by BaChem (Bubendorf, Switzerland); baclofen, barium chloride, dopamine, dynasore and strychnine by Sigma Aldrich (Poole, Dorset, UK); bicuculline, CTAP, kynurenic acid sodium salt, naloxone, PMA, sulpiride, tertiapinQ and tetrodotoxin citrate by Ascent Scientific/Abcam Biochemicals (Cambridge, UK); CGP54626, GF109203X, and norBNI by Tocris Bioscience (Bristol, UK); morphine by Macfarlan Smith (Edinburgh, UK).

Article Title: Endomorphin-2: A Biased Agonist at the ?-Opioid Receptor
Article Snippet: Morphine hydrochloride was obtained from Mcfarlan Smith (Edinburgh, UK), etorphine from Research Triangle Institute (Research Triangle Park, NC), and DAMGO from Bachem (Bubendorf, Switzerland).

Article Title: Characterization of the decrease of extracellular striatal dopamine induced by intrastriatal morphine administration
Article Snippet: Intrastriatally-administered morphine hydrochloride (supplied by the University Pharmacy, Helsinki, Finland) or DAMGO (Bachem, Switzerland) were dissolved in the Ringer solution.

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    Bachem mor agonist damgo
    Anterior insular MORs are necessary to induce mOP-LTD in the DLS. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the DLS of <t>MOR-flox</t> mice. An AAV vector encoding for cre-recombinase (AAV.hSyn.cre) was injected 8 weeks prior to recordings. Coronal brain slice showing the infection of anterior insular cortex and dorsal striatal terminal expression (bar scale = 1000 μm). b Representative electrically evoked synaptic traces and a recording time course from the DLS before and after <t>DAMGO</t> (0.3 μM, 5 min) showing the loss of mOP-LTD mediated by anterior insular MORs ( P = 0.136, t 5 = 1.775, n = 6 from 4 mice). c , d Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) and high-frequency stimulation (HFS) coupled with depolarization (4 pulses of 100 Hz, 10 s inter-pulse interval). DAMGO application was incapable of producing mOP-LTD in the DLS of anterior insula MOR knockout mice. However, HFS induced a strong reduction of eEPSCs in the DLS, indicating intact eCB-LTD (baseline vs DAMGO: P = 0.262, t 3 = 1.3.78; baseline vs HFS: P = 0.0082, t 3 = 6.259; DAMGO vs HFS: P = 0.0467, t 3 = 3.273; n = 4 from 3 mice). Data analyzed with Student’s paired t tests. Data represent mean ± SEM
    Mor Agonist Damgo, supplied by Bachem, used in various techniques. Bioz Stars score: 92/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mor agonist damgo/product/Bachem
    Average 92 stars, based on 15 article reviews
    Price from $9.99 to $1999.99
    mor agonist damgo - by Bioz Stars, 2020-09
    92/100 stars
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    Anterior insular MORs are necessary to induce mOP-LTD in the DLS. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the DLS of MOR-flox mice. An AAV vector encoding for cre-recombinase (AAV.hSyn.cre) was injected 8 weeks prior to recordings. Coronal brain slice showing the infection of anterior insular cortex and dorsal striatal terminal expression (bar scale = 1000 μm). b Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) showing the loss of mOP-LTD mediated by anterior insular MORs ( P = 0.136, t 5 = 1.775, n = 6 from 4 mice). c , d Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) and high-frequency stimulation (HFS) coupled with depolarization (4 pulses of 100 Hz, 10 s inter-pulse interval). DAMGO application was incapable of producing mOP-LTD in the DLS of anterior insula MOR knockout mice. However, HFS induced a strong reduction of eEPSCs in the DLS, indicating intact eCB-LTD (baseline vs DAMGO: P = 0.262, t 3 = 1.3.78; baseline vs HFS: P = 0.0082, t 3 = 6.259; DAMGO vs HFS: P = 0.0467, t 3 = 3.273; n = 4 from 3 mice). Data analyzed with Student’s paired t tests. Data represent mean ± SEM

    Journal: Nature Communications

    Article Title: Alcohol exposure disrupts mu opioid receptor-mediated long-term depression at insular cortex inputs to dorsolateral striatum

    doi: 10.1038/s41467-018-03683-1

    Figure Lengend Snippet: Anterior insular MORs are necessary to induce mOP-LTD in the DLS. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the DLS of MOR-flox mice. An AAV vector encoding for cre-recombinase (AAV.hSyn.cre) was injected 8 weeks prior to recordings. Coronal brain slice showing the infection of anterior insular cortex and dorsal striatal terminal expression (bar scale = 1000 μm). b Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) showing the loss of mOP-LTD mediated by anterior insular MORs ( P = 0.136, t 5 = 1.775, n = 6 from 4 mice). c , d Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) and high-frequency stimulation (HFS) coupled with depolarization (4 pulses of 100 Hz, 10 s inter-pulse interval). DAMGO application was incapable of producing mOP-LTD in the DLS of anterior insula MOR knockout mice. However, HFS induced a strong reduction of eEPSCs in the DLS, indicating intact eCB-LTD (baseline vs DAMGO: P = 0.262, t 3 = 1.3.78; baseline vs HFS: P = 0.0082, t 3 = 6.259; DAMGO vs HFS: P = 0.0467, t 3 = 3.273; n = 4 from 3 mice). Data analyzed with Student’s paired t tests. Data represent mean ± SEM

    Article Snippet: Reagents The MOR agonist DAMGO (H-2535, Bachem), MOR antagonist CTAP (H-3698, Bachem), delta opioid receptor agonist [D-Pen2 ,D-Pen5 ]-enkephalin (DPDPE; H-2905m, Bachem), α7 nicotinic acetylcholine receptor antagonist methyllycaconitine citrate (MLA; 1029, Tocris), AMPA antagonist NBQX (0373, Tocris), tetrodotoxin citrate (ARCD-0640, ARC Inc.), EtOH (E7148, Sigma-Aldrich), and GABAA receptor antagonist picrotoxin (P1675, Sigma-Aldrich) were used.

    Techniques: Slice Preparation, Mouse Assay, Plasmid Preparation, Injection, Infection, Expressing, Knock-Out

    mOP-LTD occurs at anterior insular cortex inputs to DLS and is ethanol sensitive. a Schematic figure of the injection paradigm enabling optogenetic recording from C57BL/6J DLS MSNs. An AAV vector coding for ChR2 (AAV.hSyn.ChR2) was injected 14 days prior to recordings. Coronal brain slices showing the infection of anterior insular cortex sending projections to the DLS and nucleus accumbens. Bar scales: +2.4, 200 μm; +1.7, 1000 μm; +1.2, 1000 μm; +0.1, 1000 μm. b Representative light-evoked synaptic traces from the DLS before and after DAMGO (0.3 μM, 5 min) and blocked with MOR antagonist CTAP (1 μM). c , d DAMGO application induced mOP-LTD at anterior insular terminals in the DLS and this MOR-mediated LTD was blocked by the application of CTAP ( P = 0.027, t 13 = 2.49, Control: n = 9 from 3 mice; CTAP: n = 6 from 2 mice). e Representative oEPSC traces from the DLS before and after DAMGO (0.3 μM, 5 min) application in saline (blue traces) and EtOH (red traces)-injected C57BL/6J mice. f , g EtOH exposure produced a disruption of mOP-LTD from anterior insular inputs induced by DAMGO (0.3 μM, 5 min) in the DLS ( P = 0.0046, t 9 = 3.75; Saline: n = 6 from 2 mice; EtOH: n = 5 from 3 mice). Unpaired Student’s t test. * P

    Journal: Nature Communications

    Article Title: Alcohol exposure disrupts mu opioid receptor-mediated long-term depression at insular cortex inputs to dorsolateral striatum

    doi: 10.1038/s41467-018-03683-1

    Figure Lengend Snippet: mOP-LTD occurs at anterior insular cortex inputs to DLS and is ethanol sensitive. a Schematic figure of the injection paradigm enabling optogenetic recording from C57BL/6J DLS MSNs. An AAV vector coding for ChR2 (AAV.hSyn.ChR2) was injected 14 days prior to recordings. Coronal brain slices showing the infection of anterior insular cortex sending projections to the DLS and nucleus accumbens. Bar scales: +2.4, 200 μm; +1.7, 1000 μm; +1.2, 1000 μm; +0.1, 1000 μm. b Representative light-evoked synaptic traces from the DLS before and after DAMGO (0.3 μM, 5 min) and blocked with MOR antagonist CTAP (1 μM). c , d DAMGO application induced mOP-LTD at anterior insular terminals in the DLS and this MOR-mediated LTD was blocked by the application of CTAP ( P = 0.027, t 13 = 2.49, Control: n = 9 from 3 mice; CTAP: n = 6 from 2 mice). e Representative oEPSC traces from the DLS before and after DAMGO (0.3 μM, 5 min) application in saline (blue traces) and EtOH (red traces)-injected C57BL/6J mice. f , g EtOH exposure produced a disruption of mOP-LTD from anterior insular inputs induced by DAMGO (0.3 μM, 5 min) in the DLS ( P = 0.0046, t 9 = 3.75; Saline: n = 6 from 2 mice; EtOH: n = 5 from 3 mice). Unpaired Student’s t test. * P

    Article Snippet: Reagents The MOR agonist DAMGO (H-2535, Bachem), MOR antagonist CTAP (H-3698, Bachem), delta opioid receptor agonist [D-Pen2 ,D-Pen5 ]-enkephalin (DPDPE; H-2905m, Bachem), α7 nicotinic acetylcholine receptor antagonist methyllycaconitine citrate (MLA; 1029, Tocris), AMPA antagonist NBQX (0373, Tocris), tetrodotoxin citrate (ARCD-0640, ARC Inc.), EtOH (E7148, Sigma-Aldrich), and GABAA receptor antagonist picrotoxin (P1675, Sigma-Aldrich) were used.

    Techniques: Injection, Plasmid Preparation, Infection, Mouse Assay, Produced

    MOR activation produces LTD of excitatory transmission in the dorsal striatum. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the dorsolateral striatum (DLS) of C57BL/6J mice. b Representative electrically evoked synaptic traces at baseline and after DAMGO (0.3 μM, 5 min) application. c DAMGO induced mOP-LTD of eEPSC amplitude in DLS MSNs of C57BL/6J mice ( n = 7 slices from 4 mice). d The presence of mOP-LTD is not related to alterations in series resistance. e Schematic figure of coronal brain slice showing the recording of eEPSCs by focal electric stimulation in the dorsomedial striatum (DMS). f Representative electrically evoked synaptic traces before and after DAMGO (0.3 μM, 5 min) application. g The activation of MOR by DAMGO induced LTD of eEPSC amplitude in DMS MSNs of C57BL/6J ( n = 6 from 2 mice). h The series resistance was stable during DMS recordings. Data represent mean ± SEM

    Journal: Nature Communications

    Article Title: Alcohol exposure disrupts mu opioid receptor-mediated long-term depression at insular cortex inputs to dorsolateral striatum

    doi: 10.1038/s41467-018-03683-1

    Figure Lengend Snippet: MOR activation produces LTD of excitatory transmission in the dorsal striatum. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the dorsolateral striatum (DLS) of C57BL/6J mice. b Representative electrically evoked synaptic traces at baseline and after DAMGO (0.3 μM, 5 min) application. c DAMGO induced mOP-LTD of eEPSC amplitude in DLS MSNs of C57BL/6J mice ( n = 7 slices from 4 mice). d The presence of mOP-LTD is not related to alterations in series resistance. e Schematic figure of coronal brain slice showing the recording of eEPSCs by focal electric stimulation in the dorsomedial striatum (DMS). f Representative electrically evoked synaptic traces before and after DAMGO (0.3 μM, 5 min) application. g The activation of MOR by DAMGO induced LTD of eEPSC amplitude in DMS MSNs of C57BL/6J ( n = 6 from 2 mice). h The series resistance was stable during DMS recordings. Data represent mean ± SEM

    Article Snippet: Reagents The MOR agonist DAMGO (H-2535, Bachem), MOR antagonist CTAP (H-3698, Bachem), delta opioid receptor agonist [D-Pen2 ,D-Pen5 ]-enkephalin (DPDPE; H-2905m, Bachem), α7 nicotinic acetylcholine receptor antagonist methyllycaconitine citrate (MLA; 1029, Tocris), AMPA antagonist NBQX (0373, Tocris), tetrodotoxin citrate (ARCD-0640, ARC Inc.), EtOH (E7148, Sigma-Aldrich), and GABAA receptor antagonist picrotoxin (P1675, Sigma-Aldrich) were used.

    Techniques: Activation Assay, Transmission Assay, Slice Preparation, Mouse Assay

    Anterior insular MORs are necessary to induce mOP-LTD in the DLS. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the DLS of MOR-flox mice. An AAV vector encoding for cre-recombinase (AAV.hSyn.cre) was injected 8 weeks prior to recordings. Coronal brain slice showing the infection of anterior insular cortex and dorsal striatal terminal expression (bar scale = 1000 μm). b Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) showing the loss of mOP-LTD mediated by anterior insular MORs ( P = 0.136, t 5 = 1.775, n = 6 from 4 mice). c , d Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) and high-frequency stimulation (HFS) coupled with depolarization (4 pulses of 100 Hz, 10 s inter-pulse interval). DAMGO application was incapable of producing mOP-LTD in the DLS of anterior insula MOR knockout mice. However, HFS induced a strong reduction of eEPSCs in the DLS, indicating intact eCB-LTD (baseline vs DAMGO: P = 0.262, t 3 = 1.3.78; baseline vs HFS: P = 0.0082, t 3 = 6.259; DAMGO vs HFS: P = 0.0467, t 3 = 3.273; n = 4 from 3 mice). Data analyzed with Student’s paired t tests. Data represent mean ± SEM

    Journal: Nature Communications

    Article Title: Alcohol exposure disrupts mu opioid receptor-mediated long-term depression at insular cortex inputs to dorsolateral striatum

    doi: 10.1038/s41467-018-03683-1

    Figure Lengend Snippet: Anterior insular MORs are necessary to induce mOP-LTD in the DLS. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the DLS of MOR-flox mice. An AAV vector encoding for cre-recombinase (AAV.hSyn.cre) was injected 8 weeks prior to recordings. Coronal brain slice showing the infection of anterior insular cortex and dorsal striatal terminal expression (bar scale = 1000 μm). b Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) showing the loss of mOP-LTD mediated by anterior insular MORs ( P = 0.136, t 5 = 1.775, n = 6 from 4 mice). c , d Representative electrically evoked synaptic traces and a recording time course from the DLS before and after DAMGO (0.3 μM, 5 min) and high-frequency stimulation (HFS) coupled with depolarization (4 pulses of 100 Hz, 10 s inter-pulse interval). DAMGO application was incapable of producing mOP-LTD in the DLS of anterior insula MOR knockout mice. However, HFS induced a strong reduction of eEPSCs in the DLS, indicating intact eCB-LTD (baseline vs DAMGO: P = 0.262, t 3 = 1.3.78; baseline vs HFS: P = 0.0082, t 3 = 6.259; DAMGO vs HFS: P = 0.0467, t 3 = 3.273; n = 4 from 3 mice). Data analyzed with Student’s paired t tests. Data represent mean ± SEM

    Article Snippet: The MOR agonist DAMGO (H-2535, Bachem), MOR antagonist CTAP (H-3698, Bachem), delta opioid receptor agonist [D-Pen2 ,D-Pen5 ]-enkephalin (DPDPE; H-2905m, Bachem), α7 nicotinic acetylcholine receptor antagonist methyllycaconitine citrate (MLA; 1029, Tocris), AMPA antagonist NBQX (0373, Tocris), tetrodotoxin citrate (ARCD-0640, ARC Inc.), EtOH (E7148, Sigma-Aldrich), and GABAA receptor antagonist picrotoxin (P1675, Sigma-Aldrich) were used.

    Techniques: Slice Preparation, Mouse Assay, Plasmid Preparation, Injection, Infection, Expressing, Knock-Out

    mOP-LTD occurs at anterior insular cortex inputs to DLS and is ethanol sensitive. a Schematic figure of the injection paradigm enabling optogenetic recording from C57BL/6J DLS MSNs. An AAV vector coding for ChR2 (AAV.hSyn.ChR2) was injected 14 days prior to recordings. Coronal brain slices showing the infection of anterior insular cortex sending projections to the DLS and nucleus accumbens. Bar scales: +2.4, 200 μm; +1.7, 1000 μm; +1.2, 1000 μm; +0.1, 1000 μm. b Representative light-evoked synaptic traces from the DLS before and after DAMGO (0.3 μM, 5 min) and blocked with MOR antagonist CTAP (1 μM). c , d DAMGO application induced mOP-LTD at anterior insular terminals in the DLS and this MOR-mediated LTD was blocked by the application of CTAP ( P = 0.027, t 13 = 2.49, Control: n = 9 from 3 mice; CTAP: n = 6 from 2 mice). e Representative oEPSC traces from the DLS before and after DAMGO (0.3 μM, 5 min) application in saline (blue traces) and EtOH (red traces)-injected C57BL/6J mice. f , g EtOH exposure produced a disruption of mOP-LTD from anterior insular inputs induced by DAMGO (0.3 μM, 5 min) in the DLS ( P = 0.0046, t 9 = 3.75; Saline: n = 6 from 2 mice; EtOH: n = 5 from 3 mice). Unpaired Student’s t test. * P

    Journal: Nature Communications

    Article Title: Alcohol exposure disrupts mu opioid receptor-mediated long-term depression at insular cortex inputs to dorsolateral striatum

    doi: 10.1038/s41467-018-03683-1

    Figure Lengend Snippet: mOP-LTD occurs at anterior insular cortex inputs to DLS and is ethanol sensitive. a Schematic figure of the injection paradigm enabling optogenetic recording from C57BL/6J DLS MSNs. An AAV vector coding for ChR2 (AAV.hSyn.ChR2) was injected 14 days prior to recordings. Coronal brain slices showing the infection of anterior insular cortex sending projections to the DLS and nucleus accumbens. Bar scales: +2.4, 200 μm; +1.7, 1000 μm; +1.2, 1000 μm; +0.1, 1000 μm. b Representative light-evoked synaptic traces from the DLS before and after DAMGO (0.3 μM, 5 min) and blocked with MOR antagonist CTAP (1 μM). c , d DAMGO application induced mOP-LTD at anterior insular terminals in the DLS and this MOR-mediated LTD was blocked by the application of CTAP ( P = 0.027, t 13 = 2.49, Control: n = 9 from 3 mice; CTAP: n = 6 from 2 mice). e Representative oEPSC traces from the DLS before and after DAMGO (0.3 μM, 5 min) application in saline (blue traces) and EtOH (red traces)-injected C57BL/6J mice. f , g EtOH exposure produced a disruption of mOP-LTD from anterior insular inputs induced by DAMGO (0.3 μM, 5 min) in the DLS ( P = 0.0046, t 9 = 3.75; Saline: n = 6 from 2 mice; EtOH: n = 5 from 3 mice). Unpaired Student’s t test. * P

    Article Snippet: The MOR agonist DAMGO (H-2535, Bachem), MOR antagonist CTAP (H-3698, Bachem), delta opioid receptor agonist [D-Pen2 ,D-Pen5 ]-enkephalin (DPDPE; H-2905m, Bachem), α7 nicotinic acetylcholine receptor antagonist methyllycaconitine citrate (MLA; 1029, Tocris), AMPA antagonist NBQX (0373, Tocris), tetrodotoxin citrate (ARCD-0640, ARC Inc.), EtOH (E7148, Sigma-Aldrich), and GABAA receptor antagonist picrotoxin (P1675, Sigma-Aldrich) were used.

    Techniques: Injection, Plasmid Preparation, Infection, Mouse Assay, Produced

    MOR activation produces LTD of excitatory transmission in the dorsal striatum. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the dorsolateral striatum (DLS) of C57BL/6J mice. b Representative electrically evoked synaptic traces at baseline and after DAMGO (0.3 μM, 5 min) application. c DAMGO induced mOP-LTD of eEPSC amplitude in DLS MSNs of C57BL/6J mice ( n = 7 slices from 4 mice). d The presence of mOP-LTD is not related to alterations in series resistance. e Schematic figure of coronal brain slice showing the recording of eEPSCs by focal electric stimulation in the dorsomedial striatum (DMS). f Representative electrically evoked synaptic traces before and after DAMGO (0.3 μM, 5 min) application. g The activation of MOR by DAMGO induced LTD of eEPSC amplitude in DMS MSNs of C57BL/6J ( n = 6 from 2 mice). h The series resistance was stable during DMS recordings. Data represent mean ± SEM

    Journal: Nature Communications

    Article Title: Alcohol exposure disrupts mu opioid receptor-mediated long-term depression at insular cortex inputs to dorsolateral striatum

    doi: 10.1038/s41467-018-03683-1

    Figure Lengend Snippet: MOR activation produces LTD of excitatory transmission in the dorsal striatum. a Schematic figure of coronal brain slice showing the recording of EPSCs evoked by focal electric stimulation in the dorsolateral striatum (DLS) of C57BL/6J mice. b Representative electrically evoked synaptic traces at baseline and after DAMGO (0.3 μM, 5 min) application. c DAMGO induced mOP-LTD of eEPSC amplitude in DLS MSNs of C57BL/6J mice ( n = 7 slices from 4 mice). d The presence of mOP-LTD is not related to alterations in series resistance. e Schematic figure of coronal brain slice showing the recording of eEPSCs by focal electric stimulation in the dorsomedial striatum (DMS). f Representative electrically evoked synaptic traces before and after DAMGO (0.3 μM, 5 min) application. g The activation of MOR by DAMGO induced LTD of eEPSC amplitude in DMS MSNs of C57BL/6J ( n = 6 from 2 mice). h The series resistance was stable during DMS recordings. Data represent mean ± SEM

    Article Snippet: The MOR agonist DAMGO (H-2535, Bachem), MOR antagonist CTAP (H-3698, Bachem), delta opioid receptor agonist [D-Pen2 ,D-Pen5 ]-enkephalin (DPDPE; H-2905m, Bachem), α7 nicotinic acetylcholine receptor antagonist methyllycaconitine citrate (MLA; 1029, Tocris), AMPA antagonist NBQX (0373, Tocris), tetrodotoxin citrate (ARCD-0640, ARC Inc.), EtOH (E7148, Sigma-Aldrich), and GABAA receptor antagonist picrotoxin (P1675, Sigma-Aldrich) were used.

    Techniques: Activation Assay, Transmission Assay, Slice Preparation, Mouse Assay

    Relative efficacy values for DAMGO, etorphine, endomorphin-2, and morphine for five MOPr signaling outputs. Values refer to efficacy relative to that of DAMGO, which was set to 1.00 for each output. The values for [ 35 S]GTPγS binding and arrestin-3

    Journal: Molecular Pharmacology

    Article Title: Endomorphin-2: A Biased Agonist at the ?-Opioid Receptor

    doi: 10.1124/mol.112.078659

    Figure Lengend Snippet: Relative efficacy values for DAMGO, etorphine, endomorphin-2, and morphine for five MOPr signaling outputs. Values refer to efficacy relative to that of DAMGO, which was set to 1.00 for each output. The values for [ 35 S]GTPγS binding and arrestin-3

    Article Snippet: Morphine hydrochloride was obtained from Mcfarlan Smith (Edinburgh, UK), etorphine from Research Triangle Institute (Research Triangle Park, NC), and DAMGO from Bachem (Bubendorf, Switzerland).

    Techniques: Binding Assay

    Concentration-response curves for activation of the GIRK current in rat LC neurons by DAMGO, etorphine, and endomorphin-2. In individual LC neurons, concentration-response curves for DAMGO ( n = 3–5) (A), etorphine ( n = 3–8) (B),and endomorphin-2

    Journal: Molecular Pharmacology

    Article Title: Endomorphin-2: A Biased Agonist at the ?-Opioid Receptor

    doi: 10.1124/mol.112.078659

    Figure Lengend Snippet: Concentration-response curves for activation of the GIRK current in rat LC neurons by DAMGO, etorphine, and endomorphin-2. In individual LC neurons, concentration-response curves for DAMGO ( n = 3–5) (A), etorphine ( n = 3–8) (B),and endomorphin-2

    Article Snippet: Morphine hydrochloride was obtained from Mcfarlan Smith (Edinburgh, UK), etorphine from Research Triangle Institute (Research Triangle Park, NC), and DAMGO from Bachem (Bubendorf, Switzerland).

    Techniques: Concentration Assay, Activation Assay

    Effects of exogenous opioid receptor agonists on heat hypersensitivity in wild-type and opioid peptide-lacking mice. DAMGO, DPDPE and U50, 488H were injected at the CCI site on days 2 and 14 following CCI, and effects were assessed 5 min after injection using Hargreaves test, in hind paws ipsilateral to the CCI of wild-type, END-KO, PENK-KO or PDYN-KO mice. Dashed lines represent latencies determined before CCI. # P

    Journal: Scientific Reports

    Article Title: Distinct roles of exogenous opioid agonists and endogenous opioid peptides in the peripheral control of neuropathy-triggered heat pain

    doi: 10.1038/srep32799

    Figure Lengend Snippet: Effects of exogenous opioid receptor agonists on heat hypersensitivity in wild-type and opioid peptide-lacking mice. DAMGO, DPDPE and U50, 488H were injected at the CCI site on days 2 and 14 following CCI, and effects were assessed 5 min after injection using Hargreaves test, in hind paws ipsilateral to the CCI of wild-type, END-KO, PENK-KO or PDYN-KO mice. Dashed lines represent latencies determined before CCI. # P

    Article Snippet: Substances The following substances were used: CRF, U50, 488H (Sigma Aldrich, Deisenhofen, Germany), DAMGO, DPDPE, END, ENK (Bachem, Weil am Rhein, Germany), and DYN (Tocris, Wiesbaden-Nordenstadt, Germany).

    Techniques: Mouse Assay, Injection